MYELOPATHY Flashcards

1
Q

Types of MYELOPATHY
🧠⚡ CMD⚡

A
  1. Compressive Myelopathy
    ✨ Extra medullary
    ➡️ Intradural
    ➡️ Extradural
    ✨ Intra Medullary
  2. Non-compressive Myelopathy
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2
Q

⚡⚡ MOST COMMON MYELOPATHY

A

Extramedullary Extradural

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3
Q

Extramedullary Extradural causes

A
  1. Vertebral #
  2. Disc herniation
  3. TB of Vertebra
  4. Syphilis of Vertebra
  5. Extradural abscess
  6. Metastasis in Vertebra
  7. Aneurysm
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4
Q

Extramedullary Intra-dural compressive MYELOPATHY
🧠⚡MeN have Extra ID ⚡

A

Meningioma
Neurofibroma

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5
Q

Intramedullary Compressive
Causes
🧠💡SOME💡

A

Ependymoma
Syringomyelia

Medulloblastoma
Oligodendroglioma

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6
Q

Compressive MYELOPATHY feature
@ Same Level
@ Below the level

A

⭐ LMN Motor loss, Reflexes lost, Hyperaesthesia

⭐ Complete MOTOR and SENSORY LOSS.(UMN type)

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7
Q

Pain in EXTRAMEDULLARY EXTRADURAL POSTEROLATERAL(Disc Herniation)

A

⭐ POSTEROLATERAL : RADICLE PAIN( Brief, SHOCK like Lancinating Pain)
⬇️
Lower LIMB Weakness
⬇️
Posterior Column Involvement
(Numbness and Tingling)

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8
Q

Pain in EXTRAMEDULLARY EXTRADURAL POSTERIOR Disc Herniation
Depends on:

A
  1. Posterior Column Involvement ➡️ BAND LIKE SENSATION ➕ LHERMITTE’S Sign ➕ UPPER LIMB WEAKNESS (GLOVE AND STOCKING Pattern)
  2. LATERAL COLUMN: DULL ACHING PAIN, FUNICULAR PAIN
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9
Q

INTRAMEDULLARY CORD COMPRESSION
SYRINGOMYELIA

A
  1. Bowel and Bladder Involvement
  2. Spinothalamic tract involved
  3. Sparing of DCML ➡️ DISSOCIATIVE SENSORY LOSS
  4. Pain and Temperature sensation lost: TROPHIC ULCER, CHARCOT JOINTS
  5. Anterior Horn cell Involvement LMN WEAKNESS
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10
Q

Difference BETWEEN INTRAMEDULLARY vs EXTRAMEDULLARY Cord Compression

🧠💡Intramedullary: BeST DL💡
🧠💡Extramedullary: RP² Singh💡

A
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11
Q

3Ps of CORD COMPRESSION

A
  1. Pain ➕
  2. Proteins in CSF ⬆️
  3. Pyramidal signs: EARLY
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12
Q

Proteins in CSF is ⬆️ ⬆️ when

A

ROOT Involvement is ➕

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13
Q

Epiconus vs Conus Medullaris vs CAUDA Equina
CAUDA is Asymmetric

A
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14
Q

L5 functions

A

Extensor Hallucis Longus
Hip Abduction

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15
Q

UMN type lesions are seen in CAUDA EQUINA vs CONUS MEDULLARIS?

🧠⚡ Conus - Cone of spinal cord - UMN signs ⚡
🧠⚡Cauda equina is the lower part of the spinal cord - LMN signs⚡

A

Conus Medullaris

If the conus medullaris is damaged, UMN type of lesion will occur - with hyperreflexia.

Cauda equina are nerves that exit the spinal cord.If the cauda equina is damaged, LMN type of lesion will occur - with hyporeflexia or areflexia

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16
Q

Perianal anesthesia is seen in CAUDA EQUINA vs CONUS MEDULLARIS?

🧠⚡ Conus rhymes with anus for perianal anesthesia ⚡

A

Conus Medullaris

✨ Saddle Loss
✨ Anal & Bulbocavernosus reflex LOST

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17
Q

SYMMETRY is seen in CAUDA EQUINA vs CONUS MEDULLARIS?

🧠⚡ cAudA has A’s for Asymmetric involvement ⚡

A

Cauda equina syndrome is usually asymmetric.
Conus medullaris is symmetric.

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18
Q

Bowel Bladder, Sexual Activity Involvement SEEN in CAUDA EQUINA vs CONUS MEDULLARIS?

Conus gives an early Bonus (Bowel and Bladder)

A

Conus medullaris has early onset of bowel and bladder involvement.
CES has late onset bladder involvement.

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19
Q

U/L or B/L seen in CAUDA EQUINA vs CONUS MEDULLARIS?

🧠⚡ Conus Bilateral Bonus! ⚡

A

Conus MEDULLARIS has B/L Symmetrical and SUDDEN onset

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20
Q

LOWER BACK PAIN seen in CAUDA EQUINA vs CONUS MEDULLARIS?

🧠⚡meduLLaris has two L’s for low back pain. ⚡

A

✨ Conus medullaris has low back pain. Radicular pain is absent.

✨ CES back pain is less severe. Radicular pain is present in CES.

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21
Q

🧠⚡Conus involves a conical structure ⚡

A

Conus medullaris frequently causes impotence.
In CES, impotence is absent.

22
Q

Direct Tendon Reflexes LOST seen in CAUDA EQUINA vs CONUS MEDULLARIS?

Bulbocavernosus reflex lost in both

A

Cauda Equina:
Loss of ANKLE and KNEE Reflex

Conus MEDULLARIS: Hyperreflexia
Knee reflex normal, ankle reflex lost

23
Q

MOTOR WEAKNESS seen in

A

CAUDA EQUINA
Weakness and Wasting in Thigh and Leg muscle

24
Q

Conus MEDULLARIS Sensory Distribution

A

Saddle Distribution

25
Q

ACUTE SPINAL CORD ISSUE RULES OUT WHAT TYPE OF MYELOPATHY

A

⭐ ⭐ ⭐ COMPRESSIVE MYELOPATHY IS RULED OUT

MOST PROBABLE Dx : NON COMPRESSIVE MYELOPATHY

26
Q

MOST ACUTELY PRESENTING NON COMPRESSIVE MYELOPATHY

A

Acute TRANSVERSE MYELITIS
Cause
✨ IDIOPATHIC
✨ POST INFECTIOUS
✨ POST VACCINATION

27
Q

Anterior Spinal Artery Infarction is seen in which age group

A

OLD AGE

28
Q

Approach to SPINAL CORD Involvement

A

Spinal cord involvement
💡🪔 POINTER🪔: B/L INVOLVEMENT
⬇️
SENSORY SYMPTOMS
1. ROOT PAIN / BAND LIKE PAIN ➡️ COMPRESSIVE MYELOPATHY

  1. ACUTE SPINAL FEATURES ➡️ TRANSVERSE MYELITIS
29
Q

Causes of NON COMPRESSIVE MYELOPATHY
🧠⚡VITAMIN ⚡

A

✨ VASCULAR : Anterior Spinal Artery infarct, Spinal arteriovenous malformation (AVM)

✨ INFLAMMATORY: TRANSVERSE MYELITIS, MULTIPLE SCLEROSIS

✨ TOXINS : ARSENIC

✨ AUTOIMMUNE: Sarcoidosis > > SLE

✨ METABOLIC : VITAMIN B12 DEFICIENCY

✨ INFECTION: Syphilis, TB, HIV, HTLV1

✨ NEOPLASM

✨ DEGENERATIVE : MOTOR NEURON DISEASE

SYRINGOMYELIA

30
Q

TRANSVERSE MYELITIS
💡🪔CLINICAL POINTER🪔

A

ACUTE CORD FEATURES

B/L NUMBNESS, TINGLING SENSATION

B/L COMPLETE MOTOR LOSS

PAIN, SUDDEN, SEVERE ✨ BAND LIKE ✨ AT LEVEL OF SEGMENT

Combination of SENSORY, MOTOR AND BLADDER SYMPTOMS

31
Q

Monophasic INFLAMMATORY Demyelinating Disease affecting Multiple segments of Spinal Cord

A

Transverse Myelitis

32
Q

Clinical DIAGNOSIS of TRANSVERSE MYELITIS

A

⭐ MRI : HYPER INTENSITY/ ENHANCING LESIONS

⭐ CSF Pleocytosis

⭐ INCREASED IgG INDEX

33
Q

💊💉 MANAGEMENT of TRANSVERSE MYELITIS

A
  1. STEROIDS: Mainstay TREATMENT
    methylprednisolone 500mg-1gm
  2. PLEX
34
Q

Indications of PLASMA EXCHANGE IN TRANSVERSE MYELITIS

A
  1. Inability to WALK
  2. Marked Impaired AUTONOMIC FUNCTION
  3. Sensory Loss in the LOWER EXTREMITIES
  4. No clinical improvement after 5-7 days of IV STEROIDS
35
Q

3 Conditions with
B/L ABSENCE OF KNEE JERK and ANKLE JERK

EXTENSOR PLANTAR (BABINSKI REFLEX)

🧠⚡FAST ⚡

A
  1. Friedrich’s ATAXIA
  2. Subacute DEGENERATION of Spinal Cord (Vitamin B12 deficiency)
  3. Tabes Dorsalis
36
Q
  1. Cerebellum NORMAL ➕ ATAXIA
  2. Cerebellum ATROPHY ➕ ATAXIA
A
  1. FRIEDRICH’S ATAXIA
  2. ATAXIA TELENGIECTASIA
37
Q

Commonest form of SPINOCEREBELLAR DEGENERATION

A

Friedrich’s Ataxia

38
Q

Why both UMN and LMN lesions in FRIEDRICH’S ATAXIA?

A

Spinal Cord ➕ Ganglion Disease

39
Q

1st STRUCTURE AFFECTED IN FRIEDRICH’S ATAXIA

LAST STRUCTURE AFFECTED IN FRIEDRICH’S ATAXIA

A

⭐ DORSAL ROOT GANGLION (LMN features)
⬇️
SPINOCEREBELLAR Tract DEGENERATION
⬇️
Posterior COLUMN: DCML
⬇️
CORTICOSPINAL TRACT (MOTOR)
⬇️
⭐ PERIPHERAL NERVES

40
Q

FRIEDRICH’S ATAXIA
🧠⚡IE ⚡

A

F: Frequent falls, ataxia
R: Recessive
IE:
D:Dorsal column affected - Loss of vibratory and proprioceptive sensation occurs
R: Recessive
I:
C: Cerebellar involement - Nystagmus, fast saccadic eye movements, truncal ataxia, dysarthria, dysmetria
Choreioform movements
H: Hypertrophic cardiomyopathy
High plantar arch, High steppage gait
S: Scoliosis

41
Q

Trinucleotide Repeat in FRIEDRICH’S ATAXIA
🧠⚡ATAXIA h toh GAA kar dikha ⚡

Gene involved
Chromosome

A

GAA

⭐ Frataxin Gene
⭐ Ch 9

42
Q

Non neurological features of FRIEDRICH’S ATAXIA

A
  1. Pes cavum
  2. Optic Atrophy *
  3. KyphoScoliosis
  4. Myocardial FIBROSIS
  5. Cardiomyopathy
  6. Diabetes Mellitus
  7. Hammer Toe
43
Q

Tracts involved in SCDSC

A

Posterior column
⬇️
Corticospinal tract
⬇️
Lateral Spino-Thalamic Tract

44
Q

SCDSC

A

POSTEROLATERAL cord syndrome (UMN)

NERVE ISSUES (REFLEX LOST)

45
Q

Conditions ASSOCIATED with SCDSC

A
  1. B/L OPTIC NEUROPATHY
  2. MENTAL CHANGES
46
Q

Dorsal ROOT Ganglion Involvement

Bladder Involvement

PAIN

SENSORY ATAXIA

Pupil Changes

A

Tabes Dorsalis
Bladder: OVERFLOW INCONTINENCE
Pupil: ARP

47
Q

Difference between FRIEDRICH’S ATAXIA vs TABES DORSALIS vs SCDSC

A
48
Q

ONION PEEL FACE seen in

A

SYRINGOBULBIA
DUE TO: Involvement of Spinal nucleus of TRIGEMINAL Nerve

49
Q

Syringomyelia
💡🪔CLINICAL POINTER🪔

A

♂️ > ♀️
- YOUNG ♂️
-ASSOCIATED with ARNOLD CHIARI Malformation
-DISSOCIATIVE sensory loss
- WASTING of THENAR eminence, Forearm, Arm

50
Q

HALF CAPE DISTRIBUTION seen in

A

SYRINGOMYELIA